Potassium variability during hospitalization and outcomes after discharge in patients with acute myocardial infarction

BACKGROUND The variability of metabolic biomarkers has been determined to provide incremental prognosis information,but the implications of electrolyte variability remained unclear.METHODS We investigate the relationships between electrolyte fluctuation and outcomes in survivors of acute myocardial infarction(n=4386).Ion variability was calculated as the coefficient of variation,standard deviation,variability independent of the mean(VIM)and range.Hazard ratios(HR)were estimated using the multivariable-adjusted Cox proportional regression method.RESULTS During a median follow-up of 12 months,161(3.7%)patients died,and heart failure occurred in 550(12.5%)participants after discharge,respectively.Compared with the bottom quartile,the highest quartile potassium VIM was associated with increased risks of all-cause mortality(HR=2.35,95%CI:1.36–4.06)and heart failure(HR=1.32,95%CI:1.01–1.72)independent of cardiac troponin I(c Tn I),N terminal pro B type natriuretic peptide(NT-pro BNP),infarction site,mean potassium and other traditional factors,while those associations across sodium VIM quartiles were insignificant.Similar trend remains across the strata of variability by other three indices.These associations were consistent after excluding patients with any extreme electrolyte value and diuretic use.CONCLUSIONS Higher potassium variability but not sodium variability was associated with adverse outcomes post-infarction.Our findings highlight that potassium variability remains a robust risk factor for mortality regardless of clinical dysnatraemia and dyskalaemia.

Effects of postoperative treatment with chemotherapy and cellular immunotherapy on patients with colorectal cancer

BACKGROUND The outcome of surgical treatment for colorectal cancer(CRC)remains unsatis-factory and warrants further exploration and optimization.AIM To clarify the impact of chemotherapy plus cellular immunotherapy[dendritic cell-cytokine-induced killer(DC-CIK)cell immunotherapy]on patients after CRC surgery and to explore the mediating variables.METHODS A total cohort of 121 patients who underwent CRC surgery between January 2019 and April 2022 were selected.The sample comprised a control group of 55 pa-tients who received the XELOX chemotherapy regimen and a research group of 66 patients who received XELOX+DC-CIK immunotherapy.We performed compa-rative analyses of the clinical and pathological data of the two groups,including efficacy(2-year disease-free survival[DFS]rate),the incidence of adverse events(diarrhea,myelosuppression,gastrointestinal reactions,and peripheral neuritis),serum levels of tumor markers[carcinoembryonic antigens and carbohydrate an-tigens(CA)19-9 and CA242],and T-cell subsets[cluster of differentiation(CD)3+,CD3+CD4+,CD3+CD8+,natural killer(NK),and NK T cells].We also conducted preliminary univariate and mul-tivariate analyses of the variables that affected the efficacy of the treatments.RESULTS We found a significantly higher 2-year DFS rate of treatment efficacy in the research group than in the control group,with a statistically lower incidence of adverse events.Both groups showed a reduction in serum tumor markers after treatment but there was no marked intergroup difference.After treatment,the various T-cell subgroup indicators in the control group were significantly lower than those in the research group.The indices of T-cell subsets in the research group showed no significant change from preoperative levels.Univariate analysis revealed a significant correlation between TNM staging,tumor differentiation,and the rates of nonresponse to treatment in CRC patients after surgery.Multivariate results indicated that the treatment approach significantly affected the efficacy of postoperative CRC treatment.CONCLUSION We concluded that XELOX+DC-CIK immunotherapy for postsurgical CRC patients offers reduced rates of treatment-induced adverse events,extended 2-year DFS,enhanced immunity,and increased physiological antitumor responses.